No abstract

A significant microwave selective effect on oxygen inhibition removal was found for NO decomposition through microwave catalysis over BaMn(x)Mg(1-x)O3 catalysts. Especially, the NO conversion and N2 selectivity were up to 99.8% and 99.9%, respectively for the BaMn(0.9)Mg(0.1)O3 catalyst even with the coexistence of 10% oxygen and low temperature of 250 °C.

The use of microwave (MW) irradiation to increase the rate of chemical reactions has attracted much attention recently in nearly all fields of chemistry due to substantial enhancements in reaction rates. However, the intrinsic nature of the effects of MW irradiation on chemical reactions remains unclear. Herein, the highly effective conversion of NO and decomposition of H2S via MW catalysis were investigated. The temperature was decreased by several hundred degrees centigrade. Moreover, the apparent activation energy (Ea’) decreased substantially under MW irradiation. Importantly, for the first time, a model of the interactions between microwave electromagnetic waves and molecules is proposed to elucidate the intrinsic reason for the reduction in the Ea’ under MW irradiation, and a formula for the quantitative estimation of the decrease in the Ea’ was determined. MW irradiation energy was partially transformed to reduce the Ea’, and MW irradiation is a new type of power energy for speeding up chemical reactions. The effect of MW irradiation on chemical reactions was determined. Our findings challenge both the classical view of MW irradiation as only a heating method and the controversial MW non-thermal effect and open a promising avenue for the development of novel MW catalytic reaction technology.

Preparation of catalystsCu-ZSM-5 was prepared by the ion-exchange method. H-ZSM-5 (Si/ Al = 50 supplied by Nankai University, China) was exchanged with an aqueous solution of Cu(AC) 2 (0.01 mol L À1 , AR grade, Shenyang Agent Company, China) according to the ratio of H-ZSM-5 and the aqueous solution, which was 15 g L À1 . The solution was adjusted the pH to 7 by the addition of ammonia and stirred for 12 h at 50 8C. After it was collected by filtration, the sample was washed with deionized water and dried at 100 8C for 10 h and calcined at 500 8C for 6 h. Ion exchange was performed twice to obtain a final Cu-ZSM-5 zeolite catalyst that contained 5 wt % Cu. MeO x -Cu-ZSM-5 (Me = Mn, Ni) catalysts were prepared by a mechanical mixing method. Ni 2 O 3 (AR grade, Shanghai Qiangshun Chemical Reagent Co., Ltd., China) or MnO 2 (AR grade, Taijin Fengchuan Chemical Reagent Co., Ltd., China) was added to Cu-ZSM-5, and the mixture was ground and mixed uniformly in a mortar. Catalyst characterizationXRD patterns of the samples were obtained by using a Rigaku D/ max-II/2500 X-ray powder diffractometer. CuK a radiation was employed, and the working voltage and current were 40 kV and 250 mA, respectively. FTIR spectra were recorded by using a Nicolet 380 spectrometer from 4000 to 400 cm À1 , and the KBr pellet technique was used.

No abstract

No abstract

No abstract

Quercetin is an important dietary flavonoid present in fruits and vegetables and has attracted attention because of its anti-inflammatory and anti-oxidative properties. Inflammation and oxidative stress play important roles in posttraumatic cardiomyocyte apoptosis, which contributes to secondary cardiac dysfunction. This study investigates the protective effect of quercetin on trauma-induced secondary cardiac injury and the mechanisms involved. Widely accepted nonlethal mechanical trauma models were established. In vivo, cardiomyocyte apoptosis and cardiac dysfunction in rats were assessed using TUNEL staining and a biological mechanic experiment system. In vitro, cell viability, tumour necrosis factor-α (TNF-α), reactive oxygen species (ROS) and [Ca2+]i of H9c2 cells were detected using an MTT assay, ELISA, and 2′,7′-dichlorofluorescin diacetate and fluo-4 acetoxymethyl ester assays respectively. Quercetin pretreatment (20 mg/kg i.p.; 0.5 h before trauma) significantly improved posttraumatic cardiomyocyte apoptosis and cardiac dysfunction. Pretreatment with quercetin (20 μM; 24 h before trauma plasma addition) significantly attenuated trauma-induced viability decreases, TNF-α increases, ROS overproduction and [Ca2+]i overload in H9c2 cells. In conclusion, quercetin may reverse posttraumatic cardiac dysfunction by reducing cardiomyocyte apoptosis through the suppression of TNF-α increases, ROS overproduction and Ca2+ overload in cardiomyocytes, representing a potential preventive approach for the treatment of secondary cardiac injury after mechanical trauma.